Thiopurine drugs are used as adjunct therapies for prevention of organ transplant rejection as well as in treatment of hematological neoplasias, and a variety of dermatologic, rheumatologic and neurological disorders in which the immune system is believed to play a role. Although thiopurines are very useful, relatively inexpensive drugs, they can have potentially life-threatening side effects. The metabolic conversion of thiopurine drugs to purine nucleotides and the subsequent incorporation of these derivatives into DNA plays an important role in both the efficacy and toxicity of these drugs. A competitive catabolic route for thiopurine metabolism is catalyzed by the enzyme thiopurine methyltransferase (TPMT) which inactivates thiopurines by converting them to thiomethyl derivatives such as 6-methylmercaptopurine (6-MMP). Consequently, a balance must be established between the two competing pathways such that sufficient drug is converted to the nucleotide to act as an antimetabolite, but that the level of antimetabolite does not become so high as to cause potentially harmful bone marrow suppression. In addition, TPMT activity is polymorphic in human populations, with about 89% of Caucasians and African-Americans having high activity, about 10% having intermediate activity and less than 1% having little or no activity. Patients with low TMPT activity are thus at risk for severe or fatal hematologic toxicity in response to thiopurine-based therapies. Therefore, management of patients requiring 6-MP therapy necessitates careful monitoring both before therapy begins in order to identify individuals who are more susceptible to toxic side effects, and later, during treatment to assure that 6-MP levels are maintained in a range that maximizes therapeutic efficacy while minimizing toxicity.